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细胞因子与风湿性疾病的慢性炎症。III. 类风湿关节炎中白细胞介素-2产生不足并非由于抑制机制。

Cytokines and the chronic inflammation of rheumatic disease. III. Deficient interleukin-2 production in rheumatoid arthritis is not due to suppressor mechanisms.

作者信息

Nouri A M, Panayi G S

机构信息

Rheumatology Unit, United Medical School Guy's Hospital, London England.

出版信息

J Rheumatol. 1987 Oct;14(5):902-6.

PMID:2963128
Abstract

Despite the evidence for activated T cells in the joint in rheumatoid arthritis (RA), there is evidence of deficient lymphocyte proliferation to a variety of stimulants. We investigated the production of interleukin-2 (IL-2) after phytohemagglutinin (PHA) stimulation. We show that in the peripheral blood IL-2 production was similar in RA and controls (3.7 vs 3.0 U/ml, respectively). However, blood lymphocytes from patients with joint effusions produced significantly less IL-2 than from patients without effusions (1.8 vs 5.7 U/ml, respectively). The amount of IL-2 produced by synovial fluids (SF) cells was significantly less than that produced by the corresponding blood cells (1.0 vs 1.6 U/ml). Further experiments revealed that the decreased IL-2 production was not due to its removal by IL-2 receptor positive cells in the SF and cell mixing experiments did not reveal any suppressor influences.

摘要

尽管有证据表明类风湿关节炎(RA)患者关节中的T细胞被激活,但也有证据显示淋巴细胞对多种刺激的增殖能力不足。我们研究了植物血凝素(PHA)刺激后白细胞介素-2(IL-2)的产生情况。我们发现,在类风湿关节炎患者和对照组中,外周血中IL-2的产生量相似(分别为3.7 U/ml和3.0 U/ml)。然而,有关节积液的患者血液淋巴细胞产生的IL-2明显少于无积液患者(分别为1.8 U/ml和5.7 U/ml)。滑膜液(SF)细胞产生的IL-2量明显少于相应血液细胞产生的量(分别为1.0 U/ml和1.6 U/ml)。进一步的实验表明,IL-2产生量的减少并非由于其被SF中IL-2受体阳性细胞清除,细胞混合实验也未显示出任何抑制作用。

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Clin Rheumatol. 1995 Jan;14(1):43-50. doi: 10.1007/BF02208083.
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Cellular proliferation and cytokine responses to polymethylmethacrylate particles in patients with a cemented total joint arthroplasty.
骨水泥型全关节置换术患者中细胞对聚甲基丙烯酸甲酯颗粒的增殖及细胞因子反应。
Inflamm Res. 1995 Apr;44(4):145-51. doi: 10.1007/BF01782811.
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